When MS Invades Life, Hope Survives

Multiple sclerosis pushed itself into Lynne Buckwald’s life on the morning before her 30th birthday.

She awakened with no feeling in the left side of her body. Not a tingly feeling--nothing at all.

Her symptoms soon progressed: a blind spot in her right eye, vertigo, loss of balance, fatigue--classic signs of the central-nervous-system disorder that robs people of their ability to live normal lives, to see, to walk, sometimes even to move.

Like most people, Lynne knew little about multiple sclerosis, only that it was very bad. So four months later, when my friend became one of the 350,000 Americans to be diagnosed with the disease, images of horror raced through her mind.

“My first thought was cerebral palsy and that little girl I knew as a kid who didn’t have any control over her arms and legs,” she says. “I wanted to go out and buy that new self-suicide book I read about.”

Multiple sclerosis is a chronic, often disabling disease for which there is no cure. In some ways, it is the opposite of AIDS. Instead of being deficient, the immune system works too well. For unknown reasons, it eats away at protective sheaths called myelin that surround nerves in the brain and spinal cord.

It’s as if an electrical wire’s insulation gets scraped off, short-circuiting the nerve impulses that direct muscle activity. In the mildest cases, the result is a slight lack of coordination. In the worst, paralysis occurs. About two-thirds of MS patients are women.

Thanks to the form of MS Lynne has, and some promising new drugs, her outlook is better than anything MS patients have faced before.

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Lynne Buckwald and I met on tricycles, literally, when we were both 4. We bumped into each other on the driveway feeding the street that separated our two houses in Phoenix.

Lynne became my sidekick, a forever-cheerful little girl whose exasperating love of pranks was matched only by my own. As we grew up, we did everything together, including cutting class and hiking the mountains of Arizona.

So when she called, 27 years into our friendship, to tell me she had multiple sclerosis, we mourned together too.

“You do mourn,” Lynne says. “You mourn the loss of your health.”

In the weeks after her diagnosis in Boulder, Colo., 1 1/2 years ago, Lynne went downhill. Her vision deteriorated, the vertigo got so bad she couldn’t lift her head without vomiting and she temporarily lost the ability to walk. Within a month, her marriage fell apart and she moved in with her parents in Phoenix.

It took awhile for my gregarious friend to regain control of her body. But when she did, she found strength she didn’t know she had.

Lynne was diagnosed with a relapsing form of MS; she could expect occasional flare-ups, each of which may or may not cause permanent damage, followed by periods of remission.

She began taking a new drug called Betaseron, which has been shown to reduce the frequency and intensity of flare-ups in some patients with her kind of MS.

The drug, first marketed in 1993, signaled a turning point in the fight against multiple sclerosis, and was a harbinger of more good news.

Two other promising drugs have appeared since Lynne’s diagnosis, including one reviewed by the Federal Drug Administration in September, Copaxone, which has been shown to improve neurological function.

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In a report published in July, researchers took an important step toward understanding the genetic underpinnings of MS by identifying regions in the human DNA code where MS could reside. Investigators have begun looking at how hormones may slow or speed the disease’s progression. And the once far-fetched idea of reconstituting damaged myelin has now, at least in theory, become possible.

A recent test in Oregon involving an experimental vaccine hinted at the possibility of building up cells that protect myelin.

By all accounts, MS research is moving faster than it has at any time since the disease was first written about five centuries ago. Still, the causes of the disease remain largely unknown, and a cure may be years away.

“We have turned the corner from this disease being intractable to having what looks like a very bright future,” said Dr. Fred Lublin, vice chairman of the Department of Neurology at Jefferson Medical College in Philadelphia and one of the developers of Betaseron.

On Oct. 7, an Australian and a Swiss scientist won the Nobel Prize in medicine for their immune-system research that may help treat cancer, diabetes and multiple sclerosis.

The world’s drug manufacturers have invested millions of dollars on substances such as Betaseron, Copaxone and Avonex. All three reduce the rate of relapse by about 30%.

“They’re doing it because they want to be at the table when the feeding frenzy starts,” said retired Gen. Mike Dugan, president of the National Multiple Sclerosis Society and a former chief of staff of the U.S. Air Force.

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The daughter of a Protestant minister and a schoolteacher, Lynne has been buoyed by the good news in MS research and by her strong religious faith. She has taken a job with the National Multiple Sclerosis Society in Phoenix and spends her days helping others with the disease.

“I know that despite the horrible and the unknown, ultimately MS is reawakening that sense of service in me,” she says.

Like many other MS patients, Lynne says the worst part of the disease is its unpredictability.

Patients like Lynne with relapsing forms of MS, who make up about two-thirds of the MS population, often suddenly become chronic-progressive; instead of having periodic flare-ups, they deteriorate steadily over time. Roughly 20% of MS patients fall into this latter category.

Because most research has focused on relapsing MS, which is easier to study than slow progression, there is less hope for people, like John Waters, with progressive multiple sclerosis.

But Waters, 28, of Elizabeth, N.J., whose disease has left him in a wheelchair and unable to move most of his muscles, hopes anyway--for the day his frayed myelin is repaired.

“That’s what’s going to get me walking,” he says, realizing that scientists won’t likely be able to grow myelin in humans for several years.

Most researchers want to learn how to stop the disease before concentrating on how to repair its damage, since growing new myelin is pointless if MS will destroy it anyway.

“Our whole understanding of myelin is really in its infancy, but it’s an exciting area of research,” says Patricia O’Looney, director of research and training programs at the National Multiple Sclerosis Society.

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Indeed, much MS research is in its infancy. July’s genetic study seemed to support scientists’ theory that a combination of genes and early exposure to some environmental factor causes the disease, but it also underscored how complicated MS is.

“It didn’t give us a nice neat little answer tied up in a package,” says Dr. Lael Stone, an MS researcher at the Mayo Clinic in Scottsdale, Ariz. “It gave us the sense that a lot more work needs to be done.”

Lynne now walks and moves her muscles with only slightly less agility than healthy people. But on a recent evening drive through Brooklyn, N.Y., my eternally optimistic friend confided that she is afraid.

“Will anyone want me now?” she asked me. “Am I damaged goods?”

I told her the truth, that in my eyes she is beautiful.

And when she spoke of what she wanted her life to become, somehow I knew she would find her way.

“I want to be one of those people who sets an example,” she said. “I want to show people what you can bounce back from.”

For more information about MS, call the National Multiple Sclerosis Society at (800) FIGHT-MS.